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David R. Soto-Pantoja

Researcher at Wake Forest University

Publications -  69
Citations -  7366

David R. Soto-Pantoja is an academic researcher from Wake Forest University. The author has contributed to research in topics: Medicine & Cancer. The author has an hindex of 24, co-authored 50 publications receiving 6427 citations. Previous affiliations of David R. Soto-Pantoja include National Institutes of Health.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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CD47 in the tumor microenvironment limits cooperation between antitumor T-cell immunity and radiotherapy.

TL;DR: It is reported that blocking CD47 in the context of radiotherapy enhances antitumor immunity by directly stimulating CD8(+) cytotoxic T cells, with the potential to increase curative responses.
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Radioprotection in normal tissue and delayed tumor growth by blockade of CD47 signaling.

TL;DR: Combined treatment of high-dose radiation and CD47 suppression in these translational studies suggests that a more aggressive therapeutic irradiation strategy with concurrent protection of neighboring normal tissue is possible.
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Angiotensin-(1-7) Inhibits Growth of Human Lung Adenocarcinoma Xenografts in Nude Mice through a Reduction in Cyclooxygenase-2

TL;DR: The results suggest that Ang-(1-7) may decrease COX-2 activity and proinflammatory prostaglandins to inhibit lung tumor growth and suggest that the heptapeptide represents a novel treatment for lung cancer by reducing COx-2.
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Angiotensin-(1-7) inhibits tumor angiogenesis in human lung cancer xenografts with a reduction in vascular endothelial growth factor

TL;DR: The results suggest that Ang-(1-7) may attenuate tumor angiogenesis by reducing vascular endothelial growth factor-A, a primary proangiogenic protein.